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Hydrogen gas protects IP3Rs by reducing disulfide bridges in human keratinocytes under oxidative stress.

ABSTRACT: Based on the oxidative stress theory, aging derives from the accumulation of oxidized proteins induced by reactive oxygen species (ROS) in the cytoplasm. Hydrogen peroxide (H₂O₂) elicits ROS that induces skin aging through oxidation of proteins, forming disulfide bridges with cysteine or methionine sulfhydryl groups. Decreased Ca²⁺ signaling is observed in aged cells, probably secondary to the formation of disulfide bonds among Ca²⁺ signaling-related proteins. Skin aging processes are modeled by treating keratinocytes with H₂O₂. In the present study, H₂O₂ dose-dependently impaired the adenosine triphosphate (ATP)-induced Ca²⁺ response, which was partially protected via co-treatment with ?-mercaptoethanol, resulting in reduced disulfide bond formation in inositol 1, 4, 5-trisphosphate receptors (IP₃Rs). Molecular hydrogen (H₂) was found to be more effectively protected H₂O₂-induced IP₃R1 dysfunction by reducing disulfide bonds, rather than quenching ROS. In conclusion, skin aging processes may involve ROS-induced protein dysfunction due to disulfide bond formation, and H₂ can protect oxidation of this process.

SUBMITTER: Wu CY

PROVIDER: S-EPMC5472599 | biostudies-literature | 2017 Jun

REPOSITORIES: biostudies-literature

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Hydrogen gas protects IP3Rs by reducing disulfide bridges in human keratinocytes under oxidative stress.

Wu Ching-Ying CY Hsu Wen-Li WL Tsai Ming-Hsien MH Liang Jui-Lin JL Lu Jian-He JH Yen Chia-Jung CJ Yu Hsin-Su HS Noda Mami M Lu Chi-Yu CY Chen Chu-Huang CH Yan Shian-Jang SJ Yoshioka Tohru T

Scientific reports 20170615 1

Based on the oxidative stress theory, aging derives from the accumulation of oxidized proteins induced by reactive oxygen species (ROS) in the cytoplasm. Hydrogen peroxide (H2O2) elicits ROS that induces skin aging through oxidation of proteins, forming disulfide bridges with cysteine or methionine sulfhydryl groups. Decreased Ca2+ signaling is observed in aged cells, probably secondary to the formation of disulfide bonds among Ca2+ signaling-related p ...[more]

PMID: 28620198

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Project description:Molecular hydrogen (H2) functions as an extensive protector against oxidative stress, inflammation and allergic reaction in various biological models and clinical tests; however, its essential mechanisms remain unknown. H2 directly reacts with the strong reactive nitrogen species peroxynitrite (ONOO-) as well as hydroxyl radicals (•OH), but not with nitric oxide radical (NO•). We hypothesized that one of the H2 functions is caused by reducing cellular ONOO-, which is generated by the rapid reaction of NO• with superoxides (•O2-). To verify this hypothesis, we examined whether H2 could restore cytotoxicity and transcriptional alterations induced by ONOO- derived from NO• in chondrocytes.We treated cultured chondrocytes from porcine hindlimb cartilage or from rat meniscus fibrecartilage with a donor of NO•, S-nitroso-N-acetylpenicillamine (SNAP) in the presence or absence of H2. Chondrocyte viability was determined using a LIVE/DEAD Viability/Cytotoxicity Kit. Gene expressions of the matrix proteins of cartilage and the matrix metalloproteinases were analyzed by reverse transcriptase-coupled real-time PCR method.SNAP treatment increased the levels of nitrated proteins. H2 decreased the levels of the nitrated proteins, and suppressed chondrocyte death. It is known that the matrix proteins of cartilage (including aggrecan and type II collagen) and matrix metalloproteinases (such as MMP3 and MMP13) are down- and up-regulated by ONOO-, respectively. H2 restoratively increased the gene expressions of aggrecan and type II collagen in the presence of H2. Conversely, the gene expressions of MMP3 and MMP13 were restoratively down-regulated with H2. Thus, H2 acted to restore transcriptional alterations induced by ONOO-.These results imply that one of the functions of H2 exhibits cytoprotective effects and transcriptional alterations through reducing ONOO-. Moreover, novel pharmacological strategies aimed at selective removal of ONOO- may represent a powerful method for preventive and therapeutic use of H2 for joint diseases.

Dataset Information

Hydrogen gas protects IP3Rs by reducing disulfide bridges in human keratinocytes under oxidative stress.

Publications

Hydrogen gas protects IP3Rs by reducing disulfide bridges in human keratinocytes under oxidative stress.

Similar Datasets

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